scholarly journals Gene Expression Profiling of Microdissected Pancreatic Ductal Carcinomas Using High-Density DNA Microarrays

Neoplasia ◽  
2004 ◽  
Vol 6 (5) ◽  
pp. 611-622 ◽  
Author(s):  
Robert Grützmann ◽  
Christian Pilarsky ◽  
Ole Ammerpohl ◽  
Jutta Luttges ◽  
Armin Böhme ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Dna Microarrays ◽  
High Density ◽  
Ductal Carcinomas

Preparation of Salmonella enterica Serovar Typhi Genomic DNA Microarrays for Gene Expression Profiling Analysis*

2009 ◽  
Vol 2009 (2) ◽  
pp. 206-212 ◽  
Author(s):  
Xiu-Mei SHENG ◽  
Xin-Xiang HUANG ◽  
Ling-Xiang MAO ◽  
Chao-Wang ZHU ◽  
Shun-Gao XU ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Salmonella Enterica ◽  
Genomic Dna ◽  
Dna Microarrays ◽  
Profiling Analysis

scholarly journals Gene expression profiling of wound healing in keratinocytes using DNA microarrays

10.1038/14336 ◽  
1999 ◽  
Vol 23 (S3) ◽  
pp. 54-54
Author(s):  
Claire Johnson ◽  
Frank Burslem ◽  
Jerry Lanfear
Keyword(s):  
Gene Expression ◽  
Wound Healing ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Dna Microarrays

Gene Expression Profiling Using DNA Microarrays

2013 ◽  
pp. 381-391 ◽  
Author(s):  
Kyonoshin Maruyama ◽  
Kazuko Yamaguchi-Shinozaki ◽  
Kazuo Shinozaki
Keyword(s):  
Gene Expression ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Dna Microarrays

scholarly journals In Vitro Transcription Amplification and Labeling Methods Contribute to the Variability of Gene Expression Profiling with DNA Microarrays

2006 ◽  
Vol 8 (2) ◽  
pp. 183-192 ◽  
Author(s):  
Changqing Ma ◽  
Maureen Lyons-Weiler ◽  
Wenjing Liang ◽  
William LaFramboise ◽  
John R. Gilbertson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Dna Microarrays ◽  
In Vitro Transcription

Gene expression profiling of acute cellular rejection in rat liver transplantation using DNA microarrays

2009 ◽  
Vol 15 (5) ◽  
pp. 509-521 ◽  
Author(s):  
Naoki Hama ◽  
Yuka Yanagisawa ◽  
Keizo Dono ◽  
Shogo Kobayashi ◽  
Shigeru Marubashi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Liver Transplantation ◽  
Gene Expression Profiling ◽  
Rat Liver ◽  
Expression Profiling ◽  
Dna Microarrays ◽  
Acute Cellular Rejection ◽  
Rat Liver Transplantation ◽  
Cellular Rejection

An integrated reverse functional genomic and metabolic approach to understanding orotic acid-induced fatty liver

2004 ◽  
Vol 17 (2) ◽  
pp. 140-149 ◽  
Author(s):  
Julian L. Griffin ◽  
Stephanie A. Bonney ◽  
Chris Mann ◽  
Abdul M. Hebbachi ◽  
Geoff F. Gibbons ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fatty Liver ◽  
Gene Expression Profiling ◽  
Stress Responses ◽  
Expression Profiling ◽  
Orotic Acid ◽  
Dna Microarrays ◽  
Data Sets ◽  
Functional Genomic ◽  
H Nmr

In functional genomics, DNA microarrays for gene expression profiling are increasingly being used to provide insights into biological function or pathology. To better understand the significance of the multiple transcriptional changes across a time period, the temporal changes in phenotype must be described. Orotic acid-induced fatty liver disease was investigated at the transcriptional and metabolic levels using microarrays and metabolic profiling in two strains of rats. High-resolution 1H-NMR spectroscopic analysis of liver tissue indicated that Kyoto rats compared with Wistar rats are predisposed to the insult. Metabolite analysis and gene expression profiling following orotic acid treatment identified perturbed metabolic pathways, including those involved in fatty acid, triglyceride, and phospholipid synthesis, β-oxidation, altered nucleotide, methyl donor, and carbohydrate metabolism, and stress responses. Multivariate analysis and statistical bootstrapping were used to investigate co-responses with transcripts involved in metabolism and stress responses. This reverse functional genomic strategy highlighted the relationship between changes in the transcription of stearoyl-CoA desaturase 1 and those of other lipid-related transcripts with changes in NMR-derived lipid profiles. The results suggest that the integration of 1H-NMR and gene expression data sets represents a robust method for identifying a focused line of research in a complex system.

Amplification of 6p Associated with Familial CLL

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 2432-2432
Author(s):  
Jennifer R Brown ◽  
Bethany Tesar ◽  
Megan Hanna ◽  
Megan Ash ◽  
Stacey M Fernandes ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Second Generation ◽  
Somatic Mutations ◽  
Risk Allele ◽  
Conflicts Of Interest ◽  
Snp Array ◽  
High Density ◽  
A Genome

Abstract Abstract 2432 Chronic lymphocytic leukemia (CLL) is one of the most familial of all cancers but the genetic basis of this heritability remains poorly characterized. Families with very strong inheritance of CLL have been described in the literature, and recently the occurrence of CLL in one such family was associated with a polymorphism in the DAPK gene. Here we report the genomic characterization of a family in which CLL appears to be inherited in a Mendelian autosomal dominant manner. Within this family, five of eleven siblings of the first generation were affected, and one of those affected siblings had five children, of whom three were also affected (the second generation). The children of the second generation are currently aged 20–30 and hence too young to know whether they will develop CLL. We performed high-density single-nucleotide polymorphism (SNP) array analysis and gene expression profiling on tumor and germline DNA from four of the offspring of the second generation, as well as six of their children. Analysis of the SNP array data revealed a significant germline amplification of 6p, spanning 0–720 Mb and encompassing a known copy number variant (CNV) region but significantly larger than the CNV region. This amplification was found in both affected individuals with samples available from the second generation, and was transmitted by each of them to one of their two children in the third generation. This amplification was absent from the two unaffected members of the second generation, their children, or any of the other 189 individuals with CLL who were analyzed in our high-density SNP array dataset. None of the unaffected individuals with or without the amplification had evidence of monoclonal B cell lymphocytosis (MBL) by highly sensitive flow cytometry. These unaffected individuals also lacked any PCR-detectable oligoclonal or monoclonal immunoglobulin heavy chain gene rearrangement suggestive of MBL. The region of amplification contains four protein-coding genes: EXOC2, DUSP22, HUS1B and IRF4. We sequenced the coding regions of these four genes and the 5` and 3` UTRs of IRF4 in all family members, but found no somatic mutations in this family. All four genes were also sequenced in 92 other familial CLLs, identifying no somatic mutations. We then analyzed our gene expression profiling data to assess whether any genes in this region were altered in the affected individuals with the amplification. This analysis revealed a significant 1.74X increase in IRF4 expression in the CLLs with the amplification compared to those without (q value < 0.001). By Western blotting, we confirmed that IRF4 protein was increased approximately two-fold in amplified compared to non-amplified samples. These data suggest that the amplification may target IRF4, which has been previously implicated in CLL by a genome wide association study that identified a tag SNP in its 3` UTR as a CLL risk allele. Further analysis of our SNP data demonstrated allele specific amplification in this region, and mass-spectrometric genotyping confirmed enrichment of the CLL risk allele in the individuals with amplification. We conclude that amplification of IRF4 carrying the risk allele for CLL appears likely to be the culprit predisposing to CLL in this family. Disclosures: No relevant conflicts of interest to declare.

Sign in / Sign up

Export Citation Format

Share Document